At the cellular level metabolic function is regulated by TOR kinase. TOR acts as a sensor of the cellular metabolic state and appropriately regulates metabolically-sensitive cellular processes including mitochondrial function. However, the mechanism connecting TOR to mitochondria is currently unknown. Previous work in the Rand laboratory revealed the TOR inhibitory drug rapamycin elicits different mitochondrial responses in Drosophila strains that are genetically identical except for their mitochondrial genomes. I will use genomics and proteomics as well as focused studies on known components of the TOR signaling pathway to elucidate the network of factors that mediate the rapamycin response in this system. This novel approach of using mitochondrial genome variants will provide insight into the regulation of mitochondrial function by TOR signaling and the role of the mitochondrial genome in metabolic signaling. My work has potential to reveal therapeutic targets for metabolic dysfunction in disease and shortened lifespan.